Withdrawal: Cai,H., Tao,X., Zheng,L., Huang,L., Peng,Y., Liao,R. and Zhu,Y. (2019), Ozone alleviates ischemia‐reperfusion injury by inhibiting mitochondrion‐mediated apoptosis pathway in SH‐SY5Y cells. Cell Biol Int. Accepted Author Manuscript. https://doi.org/10.1002/cbin.11087

The above article, published online on 20 December 2018 in Wiley Online Library ( https://doi.org/10.1002/cbin.11087 ), has been withdrawn by agreement with the journal Editor, Sergio Schenkman, and John Wiley & Sons Ltd. The withdrawal has been agreed because the authors have not provided a signed Copyright Transfer Agreement.     

Retraction: Citius,Altius, Fortius. J. Lange,G. Vriend. Proteins: Structure,Function, and Bioinformatics. 2020. https://doi.org/10.1002/prot.12345

The above article, published online on 12 June 2020 in Wiley Online Library ( wileyonlinelibrary.com ), has been retracted by agreement between the authors, the journal's Editor-in-Chief Dr. Nikolay Dokholyan, and John Wiley & Sons, Inc. The above article is a humorous editorial contribution surrounding a specialized topic, and was not intended for full online publication as part of the journal's scholarly content. Due to an editorial mistake, the above article was published online in Early View. John Wiley & Sons, Inc. takes full responsibility for the erroneous publication of this article.     

Retraction: Fu,W., Wang,W., Wang,H., Zhu,X., Liang,Y., Kung,H. and Zhang,J. (2014), 1,3,5‐Trihydroxy‐13,13‐dimethyl‐2H‐pyran [7,6‐b] xanthone directly targets heat shock protein 27 in hepatocellular carcinoma. Cell Biol Int, 38: 272–276. doi:10.1002/cbin.10193

The above article from Cell Biology International, published online on 07 October 2013 in Wiley Online Library ( wileyonlinelibrary.com ) has been retracted by agreement between the authors, the journal Editor‐in‐Chief and John Wiley & Sons Ltd. The retraction has been agreed due to an error in the detection method used.     

Expression of Concern: Pari,L. and Rajarajeswari,N. (2011). Antioxidant role of coumarin on streptozotocin–nicotinamide‐induced type 2 diabetic rats. J. Biochem. Mol. Toxicol., 25: 355‐361. https://doi.org/10.1002/jbt.20395

This expression of concern is for the above article, published online on May 31, 2011, in Wiley Online Library ( wileyonlinelibrary.com ), and has been published by agreement between the journal Editor‐in‐Chief, Dr Hari K. Bhat, and Wiley Periodicals, LLC. This expression of concern has been issued following concerns raised regarding the appearance of Figure 4A and the narrow range of standard deviations presented in Tables 1 and 2. The authors and the authors' institution failed to respond to a request from the Publisher and the Editor‐in‐Chief to investigate whether the images and data arose from the originally reported experiments, are unmodified, and are suitable for publication. As a result, the journal is issuing this expression of concern to readers.     

miR‐185 affected the EMT,cell viability,and proliferation via DNMT1/MEG3 pathway in TGF‐β1‐induced renal fibrosis

Kidney fibrosis is usually the final manifestation of a wide variety of renal diseases. Recent years, research reported that long non‐coding RNAs (lncRNAs) played important roles in a variety of human diseases. However, the role and underlying mechanisms of lncRNAs in kidney fibrosis were complicated and largely unclear. In our study, we constructed the cell model of renal fibrosis in HK2 cells using transforming growth factor β1 (TGF‐β1) and found that lncRNA maternally expressed gene 3 (MEG3) was downregulated in TGF‐β1‐induced renal fibrosis. We then found that overexpressed MEG3 inhibited the TGF‐β1‐induced promotion of epithelial–mesenchymal transition, cell viability, and proliferation. Furthermore, we demonstrated that DNA methyltransferases 1 (DNMT1) regulated the MEG3 expression by altering the CpGs methylation level of MEG3 promoter in TGF‐β1‐induced renal fibrosis. In addition, we further revealed that miR‐185 could regulate the DNMT1 expression and thus, modulate the MEG3 in TGF‐β1‐induced renal fibrosis. Ultimately, our study illustrated that the modulation of the miR‐185/ DNMT1/ MEG3 pathway exerted important roles in TGF‐β1‐induced renal fibrosis. In summary, our finding displayed a novel regulatory mechanism for TGF‐β1‐induced renal fibrosis, which provided a new potential therapeutic target for renal fibrosis.